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. 2019 Jun 26;10:420. doi: 10.3389/fendo.2019.00420

Figure 2.

Figure 2

Estrogen has receptor specific effects upon microglial phagocytosis. (A–C) Treatment of BV2 cells for 16 h with estradiol (E2) or selective agonists for (A) ERα (PPT), (B) ERβ (DPN) or (C) GPER (G1) revealed receptor dependent effects upon microglial phagocytosis, with activation of ERβ promoting and GPER inhibiting phagocytic activity; ERα activation had no effect on phagocytosis; data are means ± sem, n = 3, *p < 0.05 vs. untreated controls. (D) Pre-treatment of microglia with the selective ERβ antagonist PHTPP (200 nM, 15 min pre-treatment) prevented the stimulatory effect of estradiol (100 nM, 16 h) upon microglial phagocytosis of apoptotic cells; data are means ± sem, n = 3, *p < 0.05 vs. untreated controls, +p < 0.05 vs. 17β-estradiol treatment. (E) Pre-treatment of microglia with the selective GPER antagonist G1 (200 nM, 15 minute pre-treatment) enhanced the stimulatory effect of estradiol (100 nM, 16 h) upon microglial phagocytosis of apoptotic cells; data are means ± sem, n = 3, *p < 0.05 vs. untreated controls, +p < 0.05 vs. 17β-estradiol treatment. (F) Expression of all three estrogen receptors ERα, ERβ and GPER is detectable in primary murine microglia. (G) Treatment of primary murine microglia for 16 h with 17β-estradiol or DPN enhanced phagocytosis of apoptotic cells, whilst treatment with G1 inhibited phagocytosis; data are means ± sem, n = 3, *p < 0.05 vs. untreated controls, +p < 0.05 vs. 17β-estradiol treatment.